Studies of hypoxemia and pulmonary hemodynamics in acute myocardial infarction.

On 55 patients with acute myocardial infarction blood gas changes and A-aDO2 while breathing room air were observed for a period of 5 weeks. PaO2 during the 35% O2 inhalation was measured on admission and 5 weeks later for comparisons with the PaO2 while breathing room air. Pulmonary circulatory hemodynamics was measured in 29 cases on admission using Swan-Ganz's right heart flow directed catheter 7F, and the catheter was kept in the pulmonary artery in 13 cases for a maximum of 9 days. The mean PaO2 while breathing room air on admission was 66.7 mmHg in the 55 cases. It was 52.3 mmHg in the heart failure group and 74.9 mmHg in the non-heart failure group, showing prominent hypoxemia in the heart failure group. The mean PaO2 recovered to normal (84.1 mmHg and 87.0 mmHg) 5 weeks later. Inhalation of 35% O2 was performed for 20 minutes on admission and 5 weeks later. The elevation of PaO2 during the oxygen inhalation on admission was smaller than that 5 weeks later, significantly smaller in the heart failure group (P less than 0.001). The mean A-aDO2 on admission was higher in the heart failure group (58.1 mmHg) than in the non-heart failure group (34.8 mmHg). PaO2 showed significant correlations with cardiac index and SvO2. Although it was significantly correlated with PA diast. and TPR, no correlation with CVP was observed. Hypoxemia in acute myocardial infarction is caused by the following process: the onset of myocardial infarction causes low output, leading to left ventricular failure. As the result of elevated left atrial pressure and pulmonary venous pressure, intestinal pulmonary edema develops provoking ventilation-perfusion inequality, intra-pulmonary shunting, and diffusing defect.